Ishikawa S, Chang M Y, Diamond B
Department of Microbiology & Immunology, Albert Einstein College of Medicine, Bronx, NY 10461.
Immunogenetics. 1991;33(3):178-83. doi: 10.1007/BF01719237.
In an effort to generate an A.CA mouse expressing Ed, the Ead gene has been introduced into A.CA mice which lack the major histocompatibility complex (MHC) class II E molecule. Flow cytometric analysis shows cell surface expression of the E alpha chain on lymphocytes and macrophages in the transgenic mice. Analysis of T-cell receptor (Tcr) genes deleted in some E-expressing mouse strains demonstrates that T cells expressing Tcrb-V5 are partially deleted in these transgenic mice while those expressing Tcrb-V8 and Tcrb-11 are not. In addition, the expressed E alpha d chain can promote Mycoplasma arthriditis mitogen (MAM)-induced T-cell proliferation. The expression of the E alpha chain, presumably as an A beta fE alpha d heterodimer, can alter the peripheral T-cell repertoire and T-cell reactivity to a microbial superantigen.
为了培育出表达Ed的A.CA小鼠,已将Ead基因导入缺乏主要组织相容性复合体(MHC)II类E分子的A.CA小鼠体内。流式细胞术分析显示,转基因小鼠的淋巴细胞和巨噬细胞表面有Eα链表达。对一些表达E的小鼠品系中缺失的T细胞受体(Tcr)基因进行分析表明,表达Tcrb-V5的T细胞在这些转基因小鼠中部分缺失,而表达Tcrb-V8和Tcrb-11的T细胞则未缺失。此外,表达的Eαd链可促进关节炎支原体有丝分裂原(MAM)诱导的T细胞增殖。Eα链的表达,可能是以AβfEαd异二聚体的形式,可改变外周T细胞库以及T细胞对微生物超抗原的反应性。